The overall picture of Alzheimer's disease which is a major cause of dementia in elderly people and the true cause of its onset have not yet been resolved, and no fundamental method has been proposed for its prevention and treatment. As to the mechanism for its onset, an “amyloid hypothesis” has been proposed. This is now widely accepted because of pathological findings of Alzheimer's disease patients, and genetic analyses of familial Alzheimer's disease (Non-Patent Document 1).
According to this hypothesis, an unusual accumulation of a group of proteins referred to as amyloid in the brain (cerebral cortex) is related to the onset and progression of Alzheimer's disease. To put it simply, an extracellular part of a single membrane-spanning protein referred to as βAPP (β-amyloid precursor protein) is cleaved by β-secretase (β-cleavage), the fragment on the C-terminal side is then cleaved by γ-secretase (γ-cleavage), and an N-terminal fragment (β40 or β42) and a C-terminal fragment (C60 or C58 (hereinafter collectively referred to also as AICD)) are produced. Among these fragments, the N-terminal fragment (β40 or β42) has high aggregability, and form amyloid, which accumulates as senile plaques outside the cell. The production, aggregation and accumulation of amyloid cause neuronal damage, which gives rise to neuronal death.    Non-Patent Document 1: Taisuke Tomita et al., Cell Technology, 2001, Vol. 20, No. 11, p. 1489-1494